Thyroid Problems and Suggestions on Dealing with Them


While I am a German Shepherd Dog breeder, I have much all-breed experience in handling, judging, and consulting; as a scientist I also have been drawn to certain medical aspects of cynology (dog science). This said, we proceed to the subject; viz., the fairly common occurrence of impaired health that is traceable to, or at least suspected of coming from, a defective hormone production and regulatory system — specifically involving the thyroid gland. Incidentally, some readers may already know that Greyhounds, GSDs, Chow-Chows, and other breeds have greater incidence of low thyroid activity than the general or average dog population. Some breeds of dogs do better (have less “need” of as much of the hormones) than others, but enough breeds do not, especially in the low normal range. If your vet picks up a textbook that tells him your dog must be healthy because it is within that range of “low-normal”, sing to him or her from the Gershwin song, “It ain’t necessarily so!” Also, remember that the base ranges that are now considered the norm were established on Beagles, and that breeds do indeed differ in regard to their hormone needs. The list of “exceptions to the rule” has grown so much that any reliance on the old “normal” range must now be considered foolish for that growing number of breeds.

All endocrine glands are “connected”; i.e., they can influence each other’s action and efficiency. If any part of the endocrine system is out if kilter, so will be the rest. If the endocrine system is not running properly for any length of time, damage could become permanent (adrenal failure, pancreas failure, etc). Two of the most important glands in this discussion will be the pituitary and the thyroid. For a detailed discussion of the pituitary dwarfism in the GSD and related breeds, see or use a search engine [such as Google] to find my articles elsewhere on the Internet. Also, you probably should order my book on the GSD. I recommend you get the Orthopedics book at the same time.

Additionally, function in a couple of the endocrine glands can be mitigated or influenced directly by environment. So, it’s a tricky thing to adjust all these factors and treat your affected dog. Since we are discussing the thyroid in this particular article, let’s start with what it is and what it’s supposed to do, before getting into what to try to fix your problem.

In an excellent treatise on the subject some years ago, John Cargill reported:

“In the dog, the thyroid gland consists of two lobes flanking the trachea (windpipe). It has been established that it secretes at least two related hormones, thyroxine (T4) and tri-iodothyronine (T3). The only difference between the two is that T4 has four iodine atoms attached to it and T3 only has three. Even though the thyroid gland secretes mostly T4 (about 90%), it is T3 that is considered the active form of the hormone. [and…] In a series of complex steps that involve mainly the liver and kidneys, T4 is stripped of an iodine atom and is converted to T3 when needed.”


This gland has a number of functions, but the important ones can be revealed and one sees what can happen when it does not work properly: loss of haircoat (alopecia), weight gain and edema, poor heat-stress tolerance, increased dandruff, itching to the point of self-mutilation, smelly crud build-up in the ear canals, rancid body odor (especially in mature dogs), decreased fertility, lethargy, poor digestion and stool condition, possible fever, darkened skin, lowered resistance to flea infestation, or any combination of these. Insufficient hormone levels can give almost unnoticeable signs, but the experienced dog owner might pick up on them before the problem gets really bad. And a change in the environment, such as greater exposure to fleas, might shift symptoms into the frank (obvious) category.

Other signs, though less common and certainly attributable to different disorders, might include neurological symptoms such as behavioral changes (including, at worst, unprovoked aggression), head tilting, circling such as in tail chasing or appearing to search for a good spot to lie down in but never getting there), what appears to be seizures, ataxia, and lack of control of facial muscles. Remember, these are the extremes, and in most dogs you will find only the hair loss, ear crud, and one or two other indications. Abnormal behavior in dogs can have a variety of medical causes, and one might be sub-optimal thyroid function. However, behavior is very complex because it not only reflects the functioning of the whole physical and psychological organism, but it changes as a result of environmental influences.


Dr. Jean Dodds, founder of Hemopet (specialists in veterinary transfusion and blood banks), has done a great deal of work in this area. She has not gone as deeply into the effects of selenium on thyroid hormone production as others, but has made cogent observations on the connection between thyroid function and several aberrations such as behavior changes at puberty, allergies, skin problems, reaction to parasites such as fleas.

She found an increase, over the decade previous to her reports, in dogs showing various types of abnormal behavior such as aggression, extreme shyness or seizure-like activity, and that in the majority of the cases studied, significant abnormalities were found, attributable to abnormal thyroid function. The diagnosis in most of these was autoimmune thyroiditis. Her conclusion: physiological change at the cellular level leads to the aberrant behavior. She found that treatment for thyroiditis in these dogs, namely, twice daily thyroid hormone, along with a one-month tapering course of low-dose corticosteroids, successfully reversed the behavioral problems within 10 days to eight weeks.

Thyroxine treatment is apparently a good approach even without the corticosteroid, as her team found out when they had to treat a dog with facial demodectic mange; such steroids are contraindicated in demodectic mange cases. This dog got only the T4/T3 treatment: T4 at 0.1 milligram per 10 pounds plus a one-third dose of T3 at 1 microgram per pound, both given twice daily. The dog’s behavioral aggression subsided.

Dodds found also that for those animals that show occasional and not very severe seizure disorders, the thyroid medication alone usually will suffice.
She also discovered that because many of the animals with behavior problems had autoimmune thyroid disease, it was wise to avoid or minimize environmental factors that challenge the immune system. She recommended a hypoallergenic diet preserved with vitamins E and C, but without added chemical preservatives; avoiding sulfonamide antibiotics and monthly heartworm preventatives that may adversely affect the immune system; and withholding vaccination boosters until the thyroid function is balanced properly and the behavioral abnormalities are resolved. Antibody titers are far preferable to automatic revaccination schedules.


To an organic chemist such as I am (was, since I’m retired now), the two principal thyroid hormones are derivatives of an amino acid called tyrosine, containing iodine in the form of iodide ions (charged atoms). These hormones are thyroxine (also designated T4), and triiodotyronine (T3), those numbers referring to how many iodide ions are attached to each molecule. The hormone molecules consist of two tyrosine structures linked together, with iodine “stuck on” at three or four positions.

The gland secretes much more T4, but T3 is considerably more active. In other organs of the dog’s body, especially the liver and kidney, T4 is converted to T3 by stripping off one iodide ion from each molecule. T3 is quite potent, and since the healthy body makes its own in those organs, it is unwise for most people to ask that T3 supplementation be attempted. T4 is quite safe in almost any reasonable amount. Along with transthyrein and albumin, a globulin type of glycoprotein synthesized in the liver transports both through the body via the circulatory system, to where the molecules are needed by “target cells”.

One breeder-researcher-writer I corresponded with came up with an interesting analogy. He said, “T3 is the work-horse hormone. If there is a need, the pituitary gland signals the thyroid gland to send out TSH (Thyroid Stimulating Hormone); the thyroid then produces T4, which in turn is converted into T3 and other thyroid hormones. T4 is the gas at the gas station, and the T3 is putting that gas to work. This is why simply measuring the T4 levels in a dog to diagnose hypothyroidism is not correct.”

In Vet School, a student may not get as much useful data as circulates among experienced breeders. This is the case in many areas, such as breeding and reproduction, nutrition, and breed-specific health issues. For example, most vets are taught (and repeat) that young dogs don’t have thyroid hormone deficiencies, so they don’t test for this unless the owner insists. So often, the suspicions of the owner are confirmed, and the surprised vet’s eyebrows are raised twice: once at the test results and again at the remarkable recovery that often occurs in these young dogs.

I will probably keep singing the same refrain about interactions and reciprocal influence between endocrine glands, the same way I do about the interdependence of heredity and environment. Adrenal gland problems are often concomitant with thyroid problems, and “fixing the thyroid usually fixes the adrenals.” An example of hypoadrenia (sub-par adrenal gland activity) is Addison’s Disease.


I am certainly not defining my “good luck” beyond careful choice of breeding stock, but for many years I have practiced what I considered common sense: limited vaccination schedules, especially with old dogs, living in low-pollution areas, and a refusal to nearly drown dogs in every drug that the industry or vets wanted to push. I have seen much evidence of a genetic foundation for hypothyroidism (or at least the “weakness” or propensity to develop it), but I have also seen hypothyroidism appear or worsen after a failure to control fleas and the resultant flea-bite allergy (flea saliva contains antigens). The reverse is also apparently true: a dog with poor thyroid function will likely be prone to flea reaction, and a dog that has been subjected to long and overwhelming burden of contact with fleas might have its thyroids “damaged” as a result.

A recipe for health that has held up well for me for many decades of breeding has been: a well-tested & well-balanced nutrition/diet, moderation in medicine, plenty of exercise and fresh air, indoor humidifiers in winter, and watchful parasite control. Others can feed all the raw chicken, yucca, and pixie dust they want, but so far, they have not come up with any good, logical, scientific refutation for my success as a dog owner since 1937 and breeder since 1945. They can’t effectively argue with results. Nor will either camp likely convert the other. In all the hundreds of pups we’ve produced and the numerous dogs that lived their lifespans with us, I only had one that suffered from hypothyroidism and had need for regular flea control for a while and ear cleaning for a longer period. She had been sent off to travel and compete in the “care” of another professional handler (my mistake… I was too busy handling clients’ dogs to campaign her myself!) When she returned, she was in terrible condition, with the flea and thyroid condition plus a mummified puppy that was retained (she had been bred and delivered while in his hands). I bring up this incident to illustrate the complicated interaction of genetic and environmental factors in the appearance and severity of thyroid-related disorders.

In my successive roles as breeder, handler, judge, and writer, I have been witness to, and recipient of, much that deals with this subject, so I do not have to rely on my own luck or bloodlines for my data and learning. One of the lessons I have learned is that, in the best treatment for hypothyroidism, there is a range of results from barely perceptible to nearly miraculous. The treatment I refer to is the use of synthetic thyroxine. Soloxine® is one brand name; another is Synthroid®. You may also come across the Thyro-Tabs® brand, or Armour® Thyroid Tablets sold for human consumption. The website has lots of very good information, including effects on reproduction. Other informative websites are and, if these are still current. Whichever you choose, you’ll have to get a prescription from the vet, if you live in the USA.

I have seen amazing results with Soloxine in a number of health needs, especially in fleabite allergy cases and in fertility of bitches that have previously failed to conceive. Many times this temporary sterility seems to be prevented by a couple weeks of administering Soloxine. Forget the T3 tests if you just want to boost conception or try it out for frank hypothyroidism or more other minor problems such as unexplained hair loss on chest, belly, and a few other places (after you’ve positively ruled out fleas). Just convince your vet to sell you a good-size bottle and let you experiment, with his/her occasional supervision. You might ask him/her to let you start with a dosage level of about 0.1 mg (milligrams) per ten pounds of body weight. In my experience and that of many vets I have discussed it with, Soloxine (or the other brands) is extremely safe; none of them were concerned about “overdosing”.

Typically, the daily dosage is divided, the tablet halves being given orally approximately 12 hours apart, though the exact timing is not important. Some of my correspondents report satisfactory results with once-a-day doses of 0.1mg per 10 pounds, while more claim or think they need to give that much two times a day. You can either experiment with this very safe product and determine for yourself what is enough, on the basis of visually observing results, or you can help pay for your vet’s Lexus by letting him run periodic blood tests for T3/T4 levels. Perhaps every month or two until you get an idea of ideal maintenance dosage. One reason for twice-daily medication is that about half of the hormone is used and excreted from the body within 12 hours. Another is that it helps control thyroiditis by shutting off TSH production in the pituitary, and “calming down” the dog’s thyroid follicular cells and thereby inhibiting production of the antithyroid antibodies that give rise to symptoms.


A Keeshond breeder in Georgia had a 23-pound (10kg) dog that, in late middle age, reacted to its hypothyroidism with what the owner described as “paralysis” and the vet called “hypothyroid neuropathy”. Neither of them had previously seen this, although I have several similar pieces of correspondence from other owners who have had similar experience. When they finally thought of the possibility of hypothyroidism and confirmed it, the dog Rikki was started on tablets of Soloxine at 0.1mg BID (a total of 0.2mg per day). Typical of other owners, she called the symptoms “scary” and the recovery, once medication was started, as “miraculous.” The Kees never had a relapse of the paralysis (I followed up when she was elderly), not other symptoms, and the thyroid function, checked every 6 months, remained in the safe normal range.

A correspondent in the UK told me she is treating her second hypothyroid Chow-Chow, eleven years old and 35 lbs at the time of this writing, and it has been on the medicine for four years as of this writing. In her country she is using “Forthyron-400” (had used Soloxine on the previous Chow). Her story is typical of many whose vets do not recognize the symptoms as indicative of thyroid dysfunction. Here is part of what she wrote to me:

“Heaven [the first bitch] when started on the treatment was at death’s door — she was severely hypothermic (we couldn’t get a reading on the thermometer), totally uncoordinated, her eyes were ulcerated, and still the vet was diagnosing HD and entropion. I insisted she do a full set of thyroid tests – previously, when I asked her to test, she only did a simple blood test. But by the time we tested for thyroid this next time, it was almost impossible to get blood from her. Her weight had dropped to next to nothing but her head was quite puffy. The change, once medicated was amazing. We only managed to get one test, as it was so hard to take blood. Even using a needle as big as those used to insert chips, it still clogged up as soon as the blood was being drawn up the shaft.”

Speaking of this vet and her current dog, the lady said, “I think she should always test [for hypothyroidism] when there is a change in behaviour (lethargy, grumpiness) and the brittle coat with bald areas. [This] is a pretty good indication, and we have discussed this on more than one occasion.” The dog in question is related to “Heaven” — this second one’s maternal grandsire was the first bitch’s sire. Both developed severe signs well after mid-life, which follows a general pattern in my experience. I have noticed that by the time symptoms are obvious, the affected dog is usually between four and ten years of age, more often middle-aged than geriatric.

In the UK and in vet circles elsewhere, the synthetic product chemically identical to the naturally occurring T4 is referred to as levothyroxine sodium, the active soluble isomer of thyroxine. The likely reason for the vet’s confusion (other than inexperience or perhaps absence from the classroom when the lectures on hypothyroidism were delivered) was a plethora of symptoms due to the fact that basal cellular metabolism and oxygen consumption changes affecting the function of virtually all organ systems can be confusing. Especially by the time the condition has worsened without proper treatment. The dog owner must take it upon himself to “bone up” on health matters and ask specific and leading questions. See the following website if you want more about Forthyron.

On that site, the recommended starting dosage and frequency is 10 micrograms per kilogram of body weight orally every 12 hours. A kg is 2.2 pounds, so this equates to 0.1 mg (milligrams) per 2.2 lbs. of dog, or approximately 3 mg for a 66-lb. dog instead of the 0.6 to 0.7mg tablets of Soloxine that most U.S. vets would start with. Four to five times the typical American dosage. Because of variability in absorption and metabolism, the dosage may require alterations before a complete clinical response is observed, and these represent merely a starting point. Clinical results will determine how you and your vet tweak the amounts, probably even better than plasma T4 levels retested two weeks after dosage changes could, and it could take four to eight weeks to see it in the dog’s coat, behavior, etc. Once you get satisfactory results, clinical and biochemical monitoring can be performed less often, such as every 6 months or annually. Every dog is a little different, so take your lead from the patient.


Adverse effects of thyroid hormone therapy are rare and generally associated with excessive dosage, but as I mentioned, you can vary this a lot without danger. In at least one experiment, overdoses of three to six times the label-recommended starting dose for four consecutive weeks resulted in no significant clinical signs that could be attributed to treatment, which is why I refer to Soloxine as “safe”. However, chronic overdose can eventually lead to problems. Many affected dogs are on other medications, so you need to do your homework such as studying that CEVA site I referenced. One common drug perhaps too-widely prescribed is prednisone, which increases T4 binding to serum carrier proteins, so this may result in lower T4 transfer rates from serum to cellular sites where it is needed. More likely than overdosing, you may need to increase dosage if symptoms remain or return.

The following paragraph or two perhaps could be in the above section on treatments and testimonials, but I also feel the subject should be segregated. Some “alternative”, “naturopath”, or “holistic” writers, with variable levels of scientific training, understanding, credibility and qualifications, have suggested dietary preventive measures such as adding a bit of iodine-rich kelp to canine food rations, or avoiding soy (claiming it has thyroid depressant action) and not using “chemicals” to fight parasites… such latter statements really irk me, since as a chemist I decry the abysmally poor education the nation’s children have had for so many generations, under teachers who don’t seem to know that everything is composed of chemicals. These current “manglers of meaning and desecrators of definitions” usually are not careful enough to explain that what they should be complaining about is the overload of synthetic or harmful substances, an “unnatural” excess. Extremism, as Barry Goldwater said, is no vice in the defense of liberty, but it might be in the field of health.

On the other hand, there may be some “alternative” treatments that are beneficial. If you are willing to take the risk with your dog, you can investigate these. Elemental iodine compounded with potassium iodide (5 mg I with 7.5 mg KI per tablet) in a product called Iodoral or Lugol’s solution, made by Optimox, is one example, though I hesitate to mention it simply because I have no personal experience or close knowledge of its efficacy. I know Soloxine works, and though I’d prefer to get any medicines without prescriptions, I feel a little more confident going with what I know. The Iodoral has been promoted for treatment of corals in salt water aquariums, and a number of other things that make sense because of the antimicrobial (killing) effect of active iodine on a variety of fungi, bacteria, etc. But whether the Optimox iodine is actually taken up by the thyroid and used there to “repair/rejuvenate” the gland has not yet been proven to my satisfaction. I want to see double-blind control study results before giving much credibility to such reports.

Potassium iodide (KI) by itself, without the more toxic elemental iodine, is generally preferred by the medical profession for the purpose of adding dietary or medicinal iodine to the body via the gut and/or circulatory system. Elemental iodine is toxic in normally significant amounts (which is why it has been used as a disinfectant). The main reason the potassium iodide is in the formulation is probably because elemental iodine by itself is not water-soluble, but in this Lugol’s ratio, it is made so. The solution was at one time used in the treatment of gout and as a first-line treatment for iodine-deficiency hypothyroidism in adult humans. It has been used in a variety of “alternative medical” treatments for several health problems, and until 2007 was an unregulated over-the-counter product in the USA, sold as a general reagent, antiseptic, preservative, emergency disinfection of drinking water, or medicine for human or veterinary application. As of mid-2007, however, the DEA (Federal Drug Enforcement Agency) now regulates all solutions containing more than 2.2% iodine because they potentially may be used to make methamphetamine. However, as of this writing, you can still get up to one fluid ounce (30 ml) of Lugol’s exempt from this regulation in the USA. It is currently available over-the-counter in Canada and Mexico without such restrictions.

One must be very careful with dosages. Sometimes a tremendous excess can have the exact opposite effect from what the amateur administrator intended. Examples might include vitaminosis with A and D, overloading with calcium supplements that have the effect of shutting down the assimilation of that mineral, etc. If you “overdose” a dog with iodine, you could even cause the Wolff-Chaikoff effect, which is a hypothyroidism caused by ingestion of a large amount and consequent elevated levels of circulating iodide. It is referred to as autoregulatory phenomenon and inhibits formation of thyroid hormones which, of course, is opposite of what you most likely are hoping to accomplish. High levels of intracellular iodide suppress some thyroid enzymes, and reduce synthesis of thyroxine. Wolff-Chaikoff effect can be used intentionally to shut down an overactive thyroid gland, but generally in 10 days it wears off.


What about the seemingly wild claims about benefits of thyroid therapy on “other” health problems? Does Soloxine (etc.) hormone replacement/supplement truly have beneficial effects elsewhere, i.e., in connection with other disorders? Probably in many, perhaps in others. For example, this is a case report of megaesophagus successfully resolved after thyroid supplementation.

In Robert Washabau, a diplomate in internal medicine on the faculty of the U. Penn vet school, is quoted as saying, “Routine hematology, serum biochemistry, and urinalysis should be performed in all cases to investigate possible secondary causes of megaesophagus (e.g., hypothyroidism, hypoadrenocorticism). …additional diagnostic tests… thyroid function test… dogs affected with hypothyroidism should be treated with levothyroxine.” Curiously, the same man hedged a little when as a co-author of another study, they did not sound as positive, saying, “this study did not reveal a clear association between hypothyroidism and acquired megaesophagus.” J Am Vet Med Assoc. 1997 Dec 1;211(11):1406-12. Risk factors for acquired megaesophagus in dogs. Gaynor AR, Shofer FS, Washabau RJ.
Indeed, Wendy Brooks, DVM, is also at least as cautious in an article in : “Hypothyroidism may be associated with megaesophagus. It is easy to rule thyroid disease in or out with blood testing and it is important to treat a thyroid hormone deficiency; however, megaesophagus usually does not correct with thyroid replacement therapy. Whether or not hypothyroidism can truly cause megaesophagus is still being debated.” Washington State vet school, in said, “Less commonly recognized signs that may be seen in a small number of dogs with hypothyroidism include dilation of the esophagus (megaesophagus) …and abnormal ability to walk.”

A word about nutrition might be appropriate here. We know that dog food companies do a lot of blending, and geographic sources of ingredients would be impossible to report in an accurate and current manner. We also know that soil (and thus, grain and beef raised on it) varies considerably across the country in regard to such things as selenium content. Additionally, not all suppliers may be as convinced as some scientists about the need for a minimum amount of this mineral that is considered synergistic with vitamin E and other nutrients, so they may not adjust its level in their brands. Now, I fully realize that in 2008, an experimental program seemed to refute earlier claims of the benefits of vitamin E and selenium, but that study may have been flawed, and I still hold to other evidence that shows these are beneficial. The proponents of vitamin E and selenium supplementation (and I am one) will again have their day, I predict.
Here is the latest on that study: The National Cancer Institute, in 2008, cancelled a $120 million trial of 35,000 men taking selenium and vitamin E supplements as possible safeguards against prostate cancer. The trial ended four years into the projected 7-year period after scientists saw an unexpected increase in tumors among some of the men taking vitamin E, and a rise in adult-onset diabetes in some of those taking selenium. There could be other reasons for an apparent rise in incidence… one of many might be that some men taking such supplements have a false sense of security and reliance on the “miracle-vitamin”, and consequently do something stupid in some other diet or health-practice area, thinking they are invincible.

Such swings in opinion often are based on studies that are not all that well-designed in regard to eliminating other incidental causes for what results the investigators compile. For a recent example, cholesterol-lowering statin drugs were thought to yield better PSA tests in men, but lately it has been learned that they primarily reduce levels of a blood marker for prostate cancer, so it may be that they only mask the disease rather than actually lower the risk.

Another example: it seems that for a long time, every few years there is a back-or-forth reversal in whether or not chocolate, coffee, caffeine, or whatever is harmful to health. Over the years I have seen such claims and counterclaims come and go, with supposedly scientific evidence first showing one conclusion, then the opposite, then the original again, etc. The same thing has happened re saw palmetto, ginseng/ginger/gingko combinations, milk, how many cups of water one should drink each day, and many other things. If I keep to the Biblical admonition of “moderation in all things”, and the current scientific-journal evidence, plus my own observations, and balance all these, I should do OK, I think. So far, my philosophy on this has worked.

“Even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases” is a statement that comes from, along with “In areas with severe selenium deficiency there is a higher incidence…” And, also tells us, “Selenium deficiency produced up to a 14-fold decrease in hepatic T3 production from thyroxine (T4) in vitro.” In AvianWeb, we find Dr. Havashida’s study, Selenium Deficiency and Hypothyroidism. There are many more such works in the medical literature.

It must be acknowledged that there is no selenium in the thyroxine medication, and no reported level in the thyroid gland. Whether there is a direct connection or simply a beneficial effect on the whole body, or no real need for selenium in specific application to thyroid deficiency, is something that I do not think has been studied. We know that selenium is beneficial, and that Soloxine is a near-miracle drug for sick thyroids, but is there synergism or any connection? I think so, but I cannot state that as a fact backed up with scientific studies.

Complicating the picture is the apparent condition in some areas where diets contain adequate iodine but are selenium-deficient. High or normal T4 analysis may give a false sense of security, because T4 blood levels have been seen to rise when there is selenium deficiency, perhaps as a defensive reaction by the body. However, when this happens, it is often accompanied by depressed levels of T3, which is characteristic of those low-selenium, normal iodine regions.

T3 is converted by the body into T4 as needed, but it is very difficult for the dog owner to administer that without getting into toxic doses. It is much safer to give T4 and let the dog convert it internally. A few dogs are unable to do this, and these may require frequent medical monitoring by your vet. Some few dogs are able to get back to normal metabolism and do away with the need for thyroxine, but don’t count on it. If you follow up every couple of months, and see if dosage needs to be changed, long-term therapy can be very satisfactory. The good news is that Soloxine is cheap compared to most medicines, and your vet clinic visits can be spaced out further and further apart if the first months give good results.

If we learn nothing else, we should come away from a study of the endocrine system with the realization that not only do all the glands have effects on the others, but that there are many analogous biochemical interactions that teach us that the well-functioning body is a marvel of balances. Vitamins, minerals, vaccines, hormones, nutrition, medicines, genes, exercise activity — all are important to a healthy life, and in moderation, for the most part. The definition of homeostasis is appropriate here: The maintenance of steady states (you can call that “health”) in an organism by coordinated physiologic processes. Thus all organ systems are integrated by automatic adjustments to keep within narrow limits disturbances excited by, or directly resulting from, changes in the organism or its environments.

Sometimes, to restore or approach such homeostasis, we need to medicate. If you can accomplish it by careful breeding, all the better, but we live in an imperfect world, and sometimes we need a little help from our medical or chemical friends.

p.s. A typical testimonial, from GSD breeder Andrew Masia, May 2009: “It’s funny that you bring this up, because when I started breeding about 20 years ago, at the urging of Margaret Iaquinto and Al Stone, I put all my bitches on Soloxine starting about 1 month before their scheduled cycle and continuing on right up to their due date. All of the bitches were in estrus at about 16 to 20 days max with no incidents of a split heat cycle and the smallest litter that I had was 7 pups. It seems as though I have forgotten my past precautions over the last several years and I think that not so coincidentally I have recently seen more split heat cycles and smaller-sized litters. I will have to go back to the basics when my next bitch is nearing her heat. It will be interesting to see what the results will be.”
Copyright 2008 by Fred Lanting, All rights reserved, but reprinting allowed after permission. Please read his other articles: on and, for example, or e-mail him at Mr.GSD [@] for specific articles or to order his book on Canine Orthopedic Disorders or “The Total GSD”.

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